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Multiple myeloma (MM) is an incurable plasma cell neoplasm developing through long-term multistep genetic events. Biological and clinical features of MM are associated with genetic aberrations such as chromosomal translocations involving the immunoglobulin heavy chain gene locus ( IGH ) and chromosomal hyperdiploidy involving odd number chromosomes. In particular, t(11;14)(q13;q32) involving the CCND1 gene locus is characterized by lymphoplasmacytic morphology, frequent CD20 expression, an indolent clinical course, and a relatively favorable outcome in patients receiving high-dose therapy (HDT) with the aid of autologous stem cell transplantation (ASCT). 1 In contrast, t(4;14)(p16.3;q32) involving FGFR3/MMSET gene loci is associated with concomitant possession of a chromosome 13q deletion, a common IgA subtype, and a relatively unfavorable outcome even in patients receiving HDT with ASCT. However, the overall prognosis of patients with MM harboring t(4;14) is improving since the introduction of proteasome inhibitors such as bortezomib. 2 , 3 Another important chromosomal aberration observed in approximately 5% of newly diagnosed MM is t(14;16)(q32;q23) involving the c-musculoaponeurotic fibrosarcoma (c-MAF) oncogene locus. Various studies have suggested that MM carrying t(14;16) is associated with less frequent extramedullary tumor formation and hypercalcemia and an unfavorable outcome. However, this remains controversial, as the number of patients analyzed in previous reports is relatively small. 4 , 5 , 6 The aim of this study is to clarify the clinical features of patients with newly diagnosed MM (NDMM) harboring t(14;16) in Japan, especially focusing on phenotypic and karyotypic characteristics and treatment outcomes in the novel drugs era.
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Narita et al. (2015) studied this question.
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